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Inflammatory bowel disease, past, present and future: lessons from animal models.

机译:过去,现在和将来的炎症性肠病:来自动物模型的教训。

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Accumulating data from animal models indicate that Inflammatory bowel disease (IBD) is mediated by a much more complicated mechanism than previously predicted. For example, the role of an individual molecule in the pathogenesis of IBD distinctly differs depending on several factors, including the fundamental mechanism of induction of the disease, the target cell type, the phase of disease, and the environment. Therefore, it has been difficult in the past to fully explain the complicated mechanism. Novel concepts have recently been proposed to further explain the complicated mechanism of IBD. In this review, we introduce past, current, and possible future concepts for IBD models regarding T helper (Th) 1, Th2, and Th17, antigen sampling and presentation, regulatory cell networks, NOD2, Toll-like receptors, bacteria/epithelia interaction, stem cells, autophagy, microRNAs, and glycoimmunology, and we also discuss the relevance of these new concepts, developed at the bench (in animal models), to the bedside.
机译:来自动物模型的累积数据表明,炎症性肠病(IBD)是由比以前预测的机制复杂得多的机制介导的。例如,单个分子在IBD发病机理中的作用明显取决于几个因素,包括疾病诱导的基本机制,靶细胞类型,疾病阶段和环境。因此,过去很难完全解释这种复杂的机制。最近提出了新的概念来进一步解释IBD的复杂机制。在这篇综述中,我们介绍了有关IBD模型的过去,现在和将来的概念,这些概念涉及T辅助细胞(Th)1,Th2和Th17,抗原采样和呈递,调节性细胞网络,NOD2,Toll样受体,细菌/上皮细胞相互作用,干细胞,自噬,microRNA和糖免疫学,我们还将讨论在实验室(在动物模型中)开发的这些新概念与床边的相关性。

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